Evidence map›Paper›PMID 28253550›Full record

ArticleAnnals of neurology2017

Olig1 is required for noggin-induced neonatal myelin repair.

Jennifer K Sabo, Vivi Heine, John C Silbereis, Lucas Schirmer, Steven W Levison, David H Rowitch

Open access · greenAbstract read
In one paragraph

Article in Annals of neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. White matter injury after brain ischemia.Experimental neurology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 3 countries.

Jennifer K SaboDepartment of Pediatrics, Eli and Edythe Broad Center for Stem Cell Research and Regeneration Medicine, University of California, San Francisco, San Francisco, CA.
Vivi HeineDepartment of Pediatrics, Eli and Edythe Broad Center for Stem Cell Research and Regeneration Medicine, University of California, San Francisco, San Francisco, CA.
John C SilbereisDepartment of Neuroscience, University of California San Francisco, San Francisco, CA.
Lucas SchirmerEli and Edythe Broad Center for Stem Cell Research and Regeneration Medicine, University of California, San Francisco, San Francisco, CA.ORCID http://orcid.org/0000-0001-7142-4116
Steven W LevisonDepartment of Neurology and Neuroscience, New Jersey Medical School, Rutgers University-New Jersey Medical School, Newark, NJ.
David H RowitchDepartment of Pediatrics, Eli and Edythe Broad Center for Stem Cell Research and Regeneration Medicine, University of California, San Francisco, San Francisco, CA.
University of California, San Francisco · USRutgers, The State University of New Jersey · US

Funding

Regulation of Cellular Pathwaysin Human Brain DevelopmentP01NS083513 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALVAREZ-BUYLLA, ARTURO · 2014 to 2024
$12.6M
Training Program in Translational Brain Tumor ResearchT32CA151022 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2010 to 2026
$6.6M
OLIGODENDROCYTE LINEAGE GENE FUNCTION IN THE CNSR01NS040511 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROWITCH, DAVID H · 2000 to 2014
$6.4M
Glial Dysgenesis in the Injured Developing BrainR01HD052064 · NICHD · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI LEVISON, STEVEN W · 2010 to 2013
$1.4M
Medical Research Council MC_PC_12009NCI NIH HHS T32 CA151022NICHD NIH HHS R01 HD052064NINDS NIH HHS P01 NS083513NINDS NIH HHS R01 NS040511
6 · The paper itself

Abstract

objectiveNeonatal white matter injury (NWMI) is a lesion found in preterm infants that can lead to cerebral palsy. Although antagonists of bone morphogenetic protein (BMP) signaling, such as Noggin, promote oligodendrocyte precursor cell (OPC) production after hypoxic-ischemic (HI) injury, the downstream functional targets are poorly understood. The basic helix-loop-helix protein, oligodendrocyte transcription factor 1 (Olig1), promotes oligodendrocyte (OL) development and is essential during remyelination in adult mice. Here, we investigated whether Olig1 function is required downstream of BMP antagonism for response to injury in the neonatal brain.

methodsWe used wild-type and Olig1-null mice subjected to neonatal stroke and postnatal neural progenitor cultures, and we analyzed Olig1 expression in human postmortem samples from neonates that suffered HI encephalopathy (HIE).

resultsOlig1-null neonatal mice showed significant hypomyelination after moderate neonatal stroke. Surprisingly, damaged white matter tracts in Olig1-null mice lacked Olig2

interpretationThese findings indicate that Olig1 has a critical function in regulation of postnatal neural progenitor cell production in response to Noggin. Ann Neurol 2017;81:560-571.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBone Morphogenetic ProteinsCarrier ProteinsCell Culture TechniquesDisease Models, AnimalHumansHypoxia-Ischemia, BrainInfantInfant, NewbornInfant, Newborn, DiseasesMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeural Stem CellsBasic Helix-Loop-Helix ProteinsBone Morphogenetic ProteinsCarrier ProteinsNerve Tissue ProteinsNoggin ProteinOLIG1 protein, humanOlig1 protein, mouse

Identifiers

PMID28253550
PMCPMC5401646
OpenAlexW2592356009

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.